CN110729022B - Method for establishing early liver injury model of passive smoke-absorbing rat and related gene screening method - Google Patents
Method for establishing early liver injury model of passive smoke-absorbing rat and related gene screening method Download PDFInfo
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Abstract
The invention discloses a method for screening genes related to early liver injury of a rat with passive smoke, which establishes a rat passive smoke model, screens out differential genes of early liver injury of the rat with passive smoke through a liver gene chip technology, carries out annotation analysis on functions of the differential genes, and provides gene level discovery and explanation for liver injury caused by smoking.
Description
Technical Field
The invention relates to the technical field of biology, in particular to a method for screening and functional analysis of genes related to liver injury of a passive smoking rat.
Background
Smoking is a well known fact. Worldwide, as many as 250 tens of thousands die each year from smoking, smoke is the first killer of humans. The self-conscious personal hygiene habit of no smoking is developed, which is not only beneficial to health, but also is a manifestation of the public health moral. In cold smoke emitted by a smoker, the content of tobacco tar and nicotine is 1 time more than that of hot smoke inhaled by the smoker, 2 times more benzopyrene, 4 times more carbon monoxide and 50 times more ammonia.
Tobacco has been determined by the country to be a primary carcinogen. Smokers have a 10 to 30 times higher probability of lung cancer than non-smokers, with a total mortality of 90% being caused by smoking. The data show that the incidence rate of lung cancer of long-term smokers is 10-20 times higher than that of non-smokers, the incidence rate of laryngeal cancer is 6-10 times higher, and the incidence rate of coronary heart disease is 2-3 times higher. The incidence rate of the circulatory system is 3 times higher, and the incidence rate of the tracheitis is 2-8 times higher.
WHO data indicates that 300 thousands of people die annually from various diseases related to smoking are estimated to rise to 1000 tens of thousands in 2025, while China will occupy 200 tens of thousands. The smoking rate of people over 15 years old in 2002 is 35.8%, wherein the smoking rates of men and women are 66.0% and 3.1% respectively. It is estimated that smokers are about 3.5 hundred million, which is one third of the smokers worldwide. In addition, the smoking population in China has a tendency of younger, and compared with the 80 s of the 20 th century, the average age of smoking is reduced from 22.4 years old to 19.7 years old. The country is not only the country of tobacco production, but also the country of tobacco consumption. The tobacco yield in China is equivalent to the sum of the other 7 largest tobacco producing countries. The cigarettes sold in China every year are up to 1.6 trillion cigarettes, and the cigarettes consumed by people in China account for about one third of the world. If the death caused by various diseases related to smoking is counted, about 100 tens of thousands of people die each year.
The institute of respiratory and medical sciences committee Wang Chen of Beijing hospital auxiliary institution of Ministry of health indicates that smoking harm is a medical conclusion of no contention. The purpose of writing and issuing 'Chinese smoking hazard health report'. Investigation shows that the smoking population in China is over 3 hundred million, and about 7.4 hundred million people without smoking suffer from second hand smoke; the number of deaths caused by smoking related diseases exceeds 100 ten thousand per year, for example, smoking epidemic conditions are not controlled, and 300 ten thousand per year of deaths can be broken through by 2050, so that the deaths become an overwhelming burden for life health and social economic development of people. The report indicates that tobacco smoke contains 69 known carcinogens, which cause key gene mutations in the body and deregulation of the normal growth control mechanisms, ultimately leading to the development of cell carcinogenesis and malignancy.
Cigarette smoke contains over 4000 toxic chemicals that damage the liver mainly by several mechanisms: (1) direct or indirect toxic effect, promoting production of cytokines such as IL-1, IL-6, TNF-alpha, etc., causing secondary erythrocytosis, aggravating iron load and oxidative stress of serum and liver, damaging liver cells, activating hepatic stellate cells, and thereby increasing inflammatory necrosis and fibrosis of liver. (2) Immune injury: smoking can inhibit lymphocyte proliferation, accelerate lymphocyte apoptosis, and influence humoral immunity and cellular immunity of organism; (3) carcinogenesis: can inhibit T cell activity, reduce immune supervision on tumor cells, inhibit p53 gene expression, and increase tumor occurrence such as Hepatocytes (HCC). There are studies showing that smoking can increase the incidence of primary biliary cirrhosis and increase the risk of liver fibrosis in a dose-dependent manner.
Disclosure of Invention
The invention aims to establish a passive smoking infection model of rats, search liver injury difference genes of the passive smoking rats compared with normal rats by using a gene chip technology, perform functional analysis on the difference genes, and provide gene level discovery and explanation for liver injury caused by smoking.
In order to achieve the above object, the present invention provides the following technical solutions:
the invention provides a screening method of genes related to early liver injury of a passive smoke-absorbing rat, which comprises the following steps: and (3) establishing a passive smoke-absorbing rat model, screening early liver injury difference genes of the passive smoke-absorbing rat by a liver gene chip technology, and carrying out annotation analysis on functions of the genes.
Preferably, the method for establishing the passive smoking model of the rat comprises the following steps: main stream smoke exposure is carried out for 60min every day, and the smoke concentration is controlled at (1100+/-10%) mg/m 3 And the contamination is continued for 30 days.
Preferably, when the passive smoking model of the rat is built, the cigarette parameters used are as follows: 1.0 mg/branch of nicotine, 1.0 mg/branch of tar and 10.0 mg/branch of carbon monoxide.
Preferably, the chip used for detecting the rat liver gene chip is Agilent Rat lncRNA 2018.
Preferably, in the liver gene chip technology, the rat liver gene chip data is processed by adopting Feature Extraction software (version 10.7.1.1, agilent Technologies) to extract the original data, then the original data is normalized and subjected to subsequent processing by using Genespring software (version 13.1,Agilent Technologies), the normalized data is filtered, at least one group of probes with 100% marks of "P" in each group of samples for comparison is left for subsequent analysis, the fold change value is used for screening the differential genes and the differential lncRNA, and the screening standard is that the fold change value is up-regulated or down-regulated > = 2.0 and the P value is < = 0.05. Next, GO and KEGG enrichment analysis is performed on the differential gene to determine the biological function or pathway that the differential gene primarily affects.
Preferably, the early liver injury differential genes of the passive smoke rats mainly comprise: ccdc77, eef2k, slc10a2, fyn, canna 1d, samsn1, rab30, gstm6, skap1, cyp3a9, nkain4, odf2, stap1, timd4, ppara, abcg2, arhgef15, asrgl1, arl d, skap1, fggy, gimap7.
Preferably, the biological functions mainly affected by the early liver injury differential gene of the passive smoke-absorbing rat are as follows: t cell receptor signaling pathway; an organic induction; transmembrane receptor protein tyrosine kinase signaling pathway; proteolysis; negative regulation of extrinsic apoptotic signaling pathway in absence of ligand; regulation of cilium assembly; cell surface receptor signaling pathway; positive regulation of signal transduction; dendrite morphogenesis; cellular Component; termDescription; t cell receptor complex; alpha-beta T cell receptor complex; cell perithery; apical plasma membrane; cell project; cis-Golgi network; molecular Function; termDescription; phosphotyrosine binding; SH3/SH2 adapter activity; metallocarboxypeptidase activity; protease binding; lipid binding; steroid hydroxylase activity.
Preferably, the pathways mainly affected by the early liver injury differential gene of the passive smoke rats are as follows: primary immunodeficiency; hematopoietic cell lineage; chemical carcinogenesis; t cell receptor signaling pathway; prion diseases; linoleic acid metabolism; measles
In summary, compared with the prior art, the invention has the following beneficial effects:
the passive smoking rat model disclosed by the invention is subjected to exposure and contamination by mainstream smoke for 60 minutes per day, and modeling is carried out for 30 days continuously. The early liver injury genes of the passive smoke rats are screened through the liver gene-recording chip, and the functional analysis is carried out on the differential genes through GO and KEGG, so that the biological functions and the biological channels of the early liver injury differential genes of the passive smoke rats on organisms are clear.
Animals are weighed 1 time a week in the test, wherein the body weight of a model male mouse is statistically different from that of a control group on the 15 th, 22 th and 29 th days of smoke exposure (P is less than 0.05, P is less than 0.01 and P is less than 0.01); animals were dissected after 30 days, livers were extracted and weighed and organ coefficients calculated, and the results showed that the smoke exposure was 30 days, and that the liver weights of the model group male mice were lower than that of the control group, with statistical differences (P < 0.01). Experiments show that after 30 days of passive smoking, the weight of the liver and the weight of the male mice are reduced, which indicates that the model has a certain influence on the liver of animals; the gene chip result shows that the early liver injury difference genes of the rats subjected to passive smoking mainly comprise: ccdc77, eef2k, slc10a2, fyn, canna 1d, samsn1, rab30, gstm6, skap1, cyp3a9, nkain4, odf2, stap1, timd4, ppara, abcg2, arhgef15, asrgl1, arl4d, skap1, fggy, gimap7, differential gene related biological functions and pathways: primary immunodeficiency; hematopoietic cell lineage; chemical carcinogenesis; t cell receptor signaling pathway; prion diseases; linoleic acid metabolism; measles.
The passive smoking rat model established by the invention has higher scientificity, stronger reliability, accurate control of the concentration of the contaminated smoke and short modeling period, and can screen early liver injury differential genes in short time by limiting key parameters such as the type of the cigarette, the contaminated time, the contaminated method, the tar content of the cigarette and the like, thereby having great clinical significance, realizing early discovery and early prevention and taking measures.
Detailed Description
The present invention will be described in further detail with reference to specific examples. It should not be construed that the scope of the above subject matter of the present invention is limited to the following embodiments, and all techniques realized based on the present invention are within the scope of the present invention.
Examples
Establishment of passive smoking rat model
1 experimental animal: the animal species: SD rats, SPF grade, male, 24 total, age of animals at purchase: animals were purchased from beijing vernalia laboratory animal technologies limited, license number 9-10 weeks old: SCXK- (jing) 2016-0006. Animals are kept in a barrier environment (license number: SYXK (jin) 2013-0002, expiration date: 12.4.2013 to 12.4.2018, province agency: shanxi province science and technology parlor) and are kept by qualified personnel. The environmental monitoring platform is used for monitoring the room temperature and humidity of animal feeding, the room temperature is controlled at 20-26 ℃, the humidity is 40-70%, the illumination is carried out for 12 hours, and the darkness is carried out for 12 hours. The standard raising cages are used for raising, each cage is 5, and the cages are replaced 2 times per week. Cleaning after the daily operation is finished, wiping the cage frame and the table top, and wiping and sterilizing with five disinfectant solutions (glutaraldehyde solution and benzalkonium chloride) each week, and changing the types of disinfectant each week in turn. The feed is a large and small mouse feed produced by Australian feed limited company of Beijing, and the feed production license number is as follows: SCXK- (Beijing) 2014-0010. Animals were fed free diet drinking water and after 7 days of adaptive feeding, the test was started.
2 test method: 24 animals were randomly divided into control and model groups based on body weight. The model group animals are placed in a poisoning cavity, main stream smoke exposure poisoning is carried out according to the period of 60min, and the smoke concentration is controlled at (1100+/-10%) mg/m < 3 >. Animals in the control group are not infected with the toxicity, and animals in the model group are infected with the toxicity by adopting common cigarettes; the contamination frequency is 1 time per day for 30 days. Body weight was measured 1 time per week. After 30 days of contamination, all animals were subjected to gross anatomical examination, abdominal aorta was bled for blood biochemical index detection, livers were taken and weighed, and then rapidly placed in liquid nitrogen for freezing for more than 5min, and then transferred to a-80 ℃ refrigerator for storage. And then entrusts the professional detection organization to conduct genomics detection.
3 differential screening
Before screening for differential genes, probe filtration is performed, leaving at least one set of 100% probes labeled "P" in each sample group for subsequent analysis. For analyses with biological replicates, the difference significance P-value obtained by T-test and Fold difference Fold value of normalized signal values were used for screening, with the criteria Fold change value > = 2.0 and P-value < = 0.01. For analyses without biological replicates, screening was performed using Fold change values only, with the criteria Fold change values > = 2.0.
4 GO analysis
The function of the differential gene was described by GO analysis of this gene. The GO includes three major panels, biological Process, cellular Component and Molecular Function, so there are three categories of results. And counting the number of the difference genes included in each GO entry, and calculating the significance of the difference gene enrichment in each GO entry by using a statistical test method. The result of the calculation returns a P value of enrichment significance, a small P value indicating that the differential gene is enriched in the GO entry. The biological significance can be combined according to the result of GO analysis to select genes for subsequent study.
5 KEGG analysis
The Pathway analysis was performed on the differential genes using the KEGG database and statistical tests were used to calculate the significance of differential gene enrichment in each Pathway entry. The result of the calculation returns a P value of enrichment significance, a small P value indicating that the differential gene is enriched in the path. Pathway analysis has a prompting effect on experimental results, and by means of the Pathway analysis of the differential genes, pathway entries which are enriched in the differential genes can be found, and the differential genes of different samples can be found to be related to the changes of cell pathways.
6 experimental results
6.1 weight and organ weight changes
Experimental results show that the animal weights of the model group are statistically different from the comparison groups on the 15 th, 22 th and 29 th days of the flue gas exposure (P is less than 0.05, P is less than 0.01 and P is less than 0.01); animals were dissected after 30 days, livers and spleens were taken and weighed, and the results showed that the smoke exposure was 30 days, and the liver weight of the model group male mice was lower than that of the control group, and the model group male mice were statistically different (P < 0.01). The results show that after 30 days of passive smoking, the liver weight and body weight of the male mice are reduced, which indicates that the model has a certain effect on animal livers. Experimental animal body weight and organ weight results experimental results are shown in tables 1 and 2.
TABLE 1 weight variation in passively smoked rat animals
Note that: p <0.05, < P <0.01 compared to the control group.
TABLE 2 weight changes in animal organs of passively smoked rats
Note that: p <0.01 compared to the control group.
6.2 differential Gene screening
The difference significance P value obtained by T test and the Fold difference value of the normalized signal value were used for screening, the standard being Fold change value > =2.0 and P value < =0.01. For analyses without biological replicates, screening was performed using Fold change values only, with the criteria Fold change values > = 2.0. The experiment co-screened 22 differential genes, 15 of which were up-regulated and 7 of which were down-regulated, and the detailed results are shown in Table 3.
TABLE 3 screening results of liver differential Gene in passively smoked rats
6.3 differential Gene GO analysis
The function of the differential gene was described by performing GO analysis on this gene. GO includes three large panels, biological Process, cellular Component and Molecular Function. The significance of differential gene enrichment in each GO entry was calculated using statistical testing. The results of P value <0.01 are selected, and the results show that 9 biological processes related to liver difference genes of the rats subjected to passive smoking are 9, 6 cell components are related, 6 molecular functions are related, and the specific results are shown in Table 4.
TABLE 4 results of GO analysis of liver differential genes in passively smoked rats
6.4 differential Gene KEGG analysis
The Pathway analysis was performed on the differential genes using the KEGG database and statistical tests were used to calculate the significance of differential gene enrichment in each Pathway entry. The result of P value <0.01 shows that 7 pathways related to liver difference genes of the rats subjected to passive smoking are provided, and the 7 pathways mainly comprise immune, hematopoietic cell lineages, T cell receptor signaling pathways, linoleic acid metabolism and other signaling pathways, and the specific results are shown in Table 5.
TABLE 5 results of Passive smoking rat liver differential gene KEGG analysis
| TermID | TermDescription | P-value |
| path:rno053 | Primary immunodeficiency | 0.00025 |
| path:r4n0o046 | Hematopoietic cell lineage | 0.0022 |
| path:r4n0o052 | Chemical carcinogenesis | 0.0028 |
| path:r0n4o046 | T cell receptor signaling pathway | 0.0046 |
| path:r6n0o050 | Prion diseases | 0.0056 |
| path:r2n0o005 | Linoleic acid metabolism | 0.0075 |
| path:r9n1o051 | Measles | 0.0084 |
Claims (6)
1. A screening method of genes related to early liver injury of a rat with passive smoke is characterized in that a rat passive smoke model is established, and early liver injury differential genes of the rat with passive smoke are screened out by a liver gene chip technology and the functions of the genes are annotated and analyzed;
the early liver injury difference genes of the passive smoke-absorbing rats are as follows: ccdc77, eef2k, slc10a2, fyn, cacna1d, samsn1, rab30, gstm6, skap1, cyp3a9, nkain4, odf2, stap1, timd4, ppara, abcg2, arhgef15, asrgl1, arl4d, fggy, gimap;
the biological functions of the influence of the early liver injury differential genes of the passive smoke-absorbing rats are as follows: t cell receptor signaling pathway; organ induction; a transmembrane receptor protein tyrosine kinase signaling pathway; protein hydrolysis; negative regulation of extracellular signal pathways upon ligand loss; regulation of cilia assembly; cell surface receptor signaling pathways; positive regulation of signal transduction; the occurrence of dendrite morphology; a cellular component; t cell receptor complexes; an alpha-beta T cell receptor complex; cell periphery; apical plasma membrane; cell projection; a cis-golgi network; molecular function; description of the terminology; phosphotyrosine binding; SH3/SH2adaptor activity; metal carboxypeptidase activity; protease binding; lipid binding; steroid hydroxylase activity.
2. The method for screening genes related to early liver injury of a rat subjected to passive smoking according to claim 1, wherein the method for establishing a rat passive smoking model is as follows: main stream smoke exposure was performed for 60min each day, the smoke concentration was controlled at (1100.+ -. 10%) mg/m3, and exposure was continued for 30 days.
3. The method for screening genes related to early liver injury of a rat subjected to passive smoking according to claim 2, wherein when the rat is subjected to passive smoking model construction, cigarette parameters are as follows: 1.0 mg/branch of nicotine, 1.0 mg/branch of tar and 10.0 mg/branch of carbon monoxide.
4. The method for screening genes related to early liver injury of a passively smoked rat according to claim 1, wherein the liver gene chip is Agilent Rat lncRNA 2018 edition.
5. The method according to claim 4, wherein in the liver gene chip technology, the rat liver gene chip data is processed by adopting Feature Extraction software (version 10.7.1.1, agilent Technologies) to extract the original data, then the standard and subsequent processing are performed by using Genespring software (version 13.1, agilent Technologies), the standardized data is filtered, at least one group of probes with 100% marks of "P" in each group of samples for comparison is left for subsequent analysis, the differential gene and the differential lncRNA are screened by using fold change values, the screening standard is that the fold change values are up-regulated or down-regulated > = 2.0 and the P values are < = 0.05, and then the differential gene is subjected to GO and KEGG enrichment analysis to determine the biological function or pathway affected by the differential gene.
6. The method for screening early liver injury related genes of a passively smoked rat according to claim 5, wherein the pathways affected by the early liver injury differential genes of the passively smoked rat are as follows: primary immunodeficiency; hematopoietic cell lineages; chemical carcinogenesis; t cell receptor signaling pathway; prion diseases; linoleic acid metabolism; measles.
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Citations (5)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| WO2008112154A2 (en) * | 2007-03-08 | 2008-09-18 | The Hamner Institutes For Health Sciences | Methods of using genomic biomarkers to predict tumor formation |
| WO2012125712A2 (en) * | 2011-03-14 | 2012-09-20 | Respira Health, Llc | Lung tumor classifier for current and former smokers |
| CN107088223A (en) * | 2016-02-17 | 2017-08-25 | 中国人民解放军第二军医大学 | The application of Metrnl albumen or gene in treatment Endothelial dysfunction |
| CN107391962A (en) * | 2017-09-05 | 2017-11-24 | 武汉古奥基因科技有限公司 | The method of gene or site to disease regulation relationship is analysed based on multigroup credit |
| CN109601471A (en) * | 2018-10-26 | 2019-04-12 | 中国人民解放军第二军医大学 | The animal model and its application that a kind of evaluating cigarette flue gas damages mouse immune |
Family Cites Families (6)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| ES2529736T3 (en) * | 2003-04-10 | 2015-02-25 | Novartis Vaccines And Diagnostics, Inc. | Immunogenic composition comprising a SARS coronavirus spicular protein |
| EP1815245B1 (en) * | 2004-11-15 | 2010-04-21 | Erasmus MC | Prematurely ageing mouse models for the role of dna damage in ageing and intervention in ageing-related pathology |
| EP2608122A1 (en) * | 2011-12-22 | 2013-06-26 | Philip Morris Products S.A. | Systems and methods for quantifying the impact of biological perturbations |
| US20160333407A1 (en) * | 2014-07-17 | 2016-11-17 | The Brigham And Women's Hospital, Inc. | Molecular signatures of conditions associated with longevity |
| WO2018009915A1 (en) * | 2016-07-08 | 2018-01-11 | Trustees Of Boston University | Gene expression-based biomarker for the detection and monitoring of bronchial premalignant lesions |
| US10810213B2 (en) * | 2016-10-03 | 2020-10-20 | Illumina, Inc. | Phenotype/disease specific gene ranking using curated, gene library and network based data structures |
-
2019
- 2019-10-24 CN CN201911015600.4A patent/CN110729022B/en active Active
Patent Citations (5)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| WO2008112154A2 (en) * | 2007-03-08 | 2008-09-18 | The Hamner Institutes For Health Sciences | Methods of using genomic biomarkers to predict tumor formation |
| WO2012125712A2 (en) * | 2011-03-14 | 2012-09-20 | Respira Health, Llc | Lung tumor classifier for current and former smokers |
| CN107088223A (en) * | 2016-02-17 | 2017-08-25 | 中国人民解放军第二军医大学 | The application of Metrnl albumen or gene in treatment Endothelial dysfunction |
| CN107391962A (en) * | 2017-09-05 | 2017-11-24 | 武汉古奥基因科技有限公司 | The method of gene or site to disease regulation relationship is analysed based on multigroup credit |
| CN109601471A (en) * | 2018-10-26 | 2019-04-12 | 中国人民解放军第二军医大学 | The animal model and its application that a kind of evaluating cigarette flue gas damages mouse immune |
Non-Patent Citations (2)
| Title |
|---|
| "被动吸烟和饮酒对大鼠肝损伤的实验研究";王凝之，郝建宇;《医药前沿》;20180630;第8卷(第16期);第252-254页 * |
| 大鼠急性肾缺血再灌注损伤早期的基因表达;林俊毅等;《法医学杂志》;20161225;第32卷(第06期);第401-405,409页 * |
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